Understanding Blood Pressure

Blood pressure is a measurement of the force exerted upon blood vessel walls by blood as it flows through the arteries. High blood pressure occurs when there is an increase of force against the arterial wall, with potentially damaging consequences. Since the heart has distinct “beats”, the pressure of oxygenated blood in the arteries is not continuous, but varies between two values, one when the heart is contracting, and one when the heart is relaxing. As the heart contracts, blood is expelled from the left ventricle under the greatest force; this upper pressure limit is the systolic blood pressure.

Following contraction of the heart, the aortic valve closes, which prevents blood from flowing backward into the heart, and helps maintain pressure in the arteries. This allows the heart muscle to relax and fill with blood. Unlike all other organs, which receive blood flow when the heart “beats” or contracts, the heart itself is unique in that it receives blood supply between heartbeats. As the heart contracts to pump blood to the rest of the body, circulation to the heart itself is impeded. Blood pressure during the heart’s “resting” period between contractions, called diastole, must be sufficient to deliver an adequate supply of oxygenated blood to cardiac tissue. In aging individuals with pre-existing coronary artery disease and/ or long-standing high blood pressure, overly-aggressive reduction of diastolic blood pressure can reduce the delivery of oxygenated blood to the heart. The diastolic blood pressure should be close to 75 mmHg for optimal health.

The alternation between systolic and diastolic blood pressure occurs with every heartbeat, some 60-80 times per minute in the average adult at rest. Clinically, blood pressure measurements are expressed, in millimeters of mercury (mmHg), as the ratio of systolic pressure over diastolic pressure (e.g., 120/80 mmHg).

For most aging individuals, Life Extension recommends an optimal blood pressure goal of 115/75 mmHg. However, those aging individuals with long-standing hypertension and/ or coronary artery disease should be aware that a rapid, overly-aggressive reduction of blood pressure, in particular diastolic blood pressure, should be avoided.

How Is Blood Pressure Regulated?

Blood pressure in the circulatory system is controlled three ways: 1) The force and rate at which blood leaves the heart (cardiac output); 2) the diameter and flexibility of the blood vessels though which blood flows (peripheral resistance); and 3) the total volume of blood in the circulatory system. All three work in concert to maintain a steady long-term pressure, while allowing for short-term increases to address cardiovascular needs.

Increasing the rate at which the heart beats, and the force at which blood leaves the heart results in a greater flow of blood and an increase in pressure; thus allowing the short-term increase in circulation that may be necessary during exercise, or in adapting to stress. Increases in cardiac output can be triggered by signals from the brain, or in response to stress hormones, such as epinephrine (adrenaline).

Peripheral resistance describes the increase in blood pressure caused by blood vessels themselves. The more resistance to blood flow, the greater the amount of blood pressure needed to overcome this resistance. Arteries actively modulate their resistance by constriction, which decreases the diameter of the vessel (vasoconstriction) and increases blood pressure, or dilation (vasodilation), which lowers resistance and blood pressure. Vasoconstriction and vasodilation are also short-term mechanisms to regulate blood pressure, and are under the control of several hormones. Aging causes arteries to lose their elasticity, which explains why the majority of aging people have above optimal blood pressure readings. Since it is “normal” for people’s blood pressure to rise with age, interventions are usually required to keep it in safe ranges. People should not be surprised to learn that they need to take steps to bring their blood pressure under control – it is a part of normal aging for most of us.

The last mechanism for blood pressure regulation is through blood volume. Blood is a suspension of cells in an aqueous medium; its volume can therefore be modified by altering its water content. Increasing the amount of water in the blood increases volume and the pressure it exerts. Reducing water content lowers blood pressure. Changes in blood volume are long-term mechanisms for blood pressure control.

Aside from the influence of neural triggers on heart rate, much of blood pressure control is performed by the kidneys. By controlling the balance of water and salt, the kidneys influence blood volume, lending long-term blood pressure control. The kidneys also produce hormones that act remotely to increase blood pressure through vasoconstriction of arteries. Kidney function can become impaired as people age, which is another reason why blood pressure may increase as we grow older. A major reason for kidney impairment is hypertension, so those starting with mild kidney problems have elevated blood pressure that then inflicts more kidney damage resulting in still higher blood pressure readings. Excess blood glucose (above 99 mg/dL) is another major cause of kidney damage. Fasting glucose levels should be kept below86 mg/dL for overall disease prevention (optimal range: 70 to 85 mg/dL).

Central to the kidney’s control of blood pressure is the renin-angiotensin-aldosterone system, a hormone system that work together to control blood pressure. Renin is an enzyme produced in the kidneys in response to low blood volume, depletion of sodium chloride, and stress. The production of renin leads, in turn, to the production of angiotensin II, a hormone that increases blood pressure. Angiotensin II increases blood pressure in the following ways:

causing the kidneys to retain sodium and water, which increases blood volume

causing the vasoconstriction of small blood vessels, which increases arterial blood pressure

inhibiting bradykinin (i.e., a hormone that relaxes blood vessels)

stimulating the production of additional hypertensive (blood pressure raising) hormones in the adrenal and pituitary glands

indirectly acting on the central nervous system to increase thirst and the craving for salt, both of which are necessary for increasing blood volume.

In recent years, researchers have made tremendous strides in understanding the connection between high blood pressure and various cardiovascular diseases. It turns out that elevated blood pressure damages arteries at a basic level—the endothelium. Endothelial dysfunction is linked with the development of cardiovascular events.

Arteries are made up of three layers. The outer layer is mostly connective tissue that provides support to the inner two layers. The middle layer is smooth muscle that contracts and expands to facilitate circulation and maintain optimal blood pressure. The inner layer, or endothelium, is composed of a thin layer of cells that protects the integrity of the artery, promotes blood clotting in case of injury, and helps prevent damaging molecules such as low-density lipoproteins (LDLs) and triglycerides from penetrating the wall of the artery. When the endothelial layer is damaged, the result can be a thickened arterial wall and the abnormal aggregation of white blood cells. Sensing an injury, the endothelium stimulates a healing response that ultimately leads to an atherosclerotic plaque (Versari 2009; Rocha 2010).

Elevated blood pressure has been shown to contribute significantly to endothelial dysfunction. High blood pressure causes functional alterations in the endothelium that, in turn, are associated with decreased arterial mobility and increased stiffness in the arterial wall (Hausberg 2005). When the arteries become “stiff” or hardened, and can no longer contract and dilate sufficiently, additional stress is placed on the heart's main pumping chamber, the left ventricle. As a result, the left ventricle may be enlarged (left ventricular hypertrophy) (Palmieri 2005). Left ventricular hypertrophy is often the first sign that damage from uncontrolled high blood pressure has started to occur (Kannel 1995). If left untreated, ventricular hypertrophy may evolve into congestive heart failure.

The degree of endothelial dysfunction correlates with target organ damage (Xu 2009). As a result, physicians measure the effects of high blood pressure by looking at target organ damage. In other words, treatment decisions are based on how much damage high blood pressure is causing to organs such as the kidneys, eyes, or heart.

The intimate relationship that exists between high blood pressure and endothelial dysfunction highlights the need to address both of these phenomena as separate, yet unified contributors to cardiovascular disease. In fact, the network of interrelated cardiovascular risk factors includes a myriad of additional components that must be addressed to truly reduce cardiovascular risk. More information on the multifactorial nature of cardiovascular disease can be found in the Life Extension Magazine article entitled How to Circumvent 17 Independent Heart Attack Risk Factors.

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